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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1975, France will have manufactured 3.2 million tons of plastic materials which by pyrolysis, liberate chlorine, methyl chloride, hydrocyanic acid, hydrofluoric acid and other toxic gases. Now these materials are burnt in fires in "modern", buildings or vehicles , associated with fats (acrolein) and other gases and toxic industrial or household fumes which attack the lung. At sufficient dosage these agressive agents have first of all a "suffocating" action when in case of survival, a caustic and corrosive action. Pulmonary edema of the lesional type is met with at two stages in these cases. They are due to a direct action on the bronchial epithelium and an indirect action by disturbance of surfactant metabolism. It is an edema which is interstitial above all, and secondarily endo-alveolar. Study of the clinical, radiological, bronchoscopic and hemodynamic symptomatology. Differential diagnosis is not always easy. The possibility of burns of the respiratory pathways, blast, must be looked at. These elements can moreover be associated with lesions due to toxic inhalation. In case of survival the course is one of fibrosis with a restrictive syndrome.
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PMID:[Pulmonary edema due to inhalation of gas and vapors]. 0 77

Eighty-two patients were hospitalized following an accidental exposure to chlorine. All patients presented with dyspnoea and cough. The other symptoms included irritation of throat (53.6%), irritation of eyes (42.3%), headache (29.2%), abdominal pain (26.8%), vomiting (24.3%) and giddiness (9.7%). All of them had bronchospasm and 5 (6%) had cyanosis at the onset. An x-ray of the chest revealed patchy infiltrates in 3 (3.85%) and hilar congestion in 2 (2.44%). Pulmonary function tests showed an obstructive pattern in 27.4%, restrictive in 3.25% and mixed in 53.2%. Pulmonary functions were normal in 16.1% of the patients. Bronchoscopy revealed tracheobronchial mucosal congestion in all cases, hemorrhagic spots in 35.7%, erosions and ulcers in 12.5%. All patients were treated with oxygen, aminophylline, hydrocortisone and antibiotics. Haematemesis (n = 1) and pulmonary oedema (n = 2) developed 12 hours after the admission. Two other patients developed pneumonia 48 hours later. All patients recovered satisfactorily. On follow-up 16 patients had no sequelae after one year. Pulmonary functions were normal in 5 patients after 3 years of follow-up.
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PMID:Acute accidental exposure to chlorine fumes--a study of 82 cases. 145 67

Chlorine inhalation may rapidly cause pulmonary edema, leading to acute hypoxemic respiratory failure. We report a 12 year old with acute respiratory failure from inhalation injury after he accidentally dropped chlorine tablets into a swimming pool. Supplemental oxygen alone failed to provide adequate arterial oxygenation. We administered positive end expiratory pressure (PEEP) in the emergency department, resulting in markedly improved oxygenation. Early institution of PEEP should be considered in patients with chlorine poisoning when supplemental oxygen alone is insufficient.
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PMID:Treatment of acute hypoxemic respiratory failure caused by chlorine exposure. 188 8

While chlorine gas inhalation has previously been reported to cause temporary mucous membrane irritation, acute pneumonitis, pulmonary edema, and transient bronchospasm, there is controversy about the existence of long-term pulmonary sequelae. We report the case of a 25-year-old man in whom chronic, recurrent asthma developed after exposure to a chlorine gas leak in an enclosed space. His course since the exposure has been notable for frequent exacerbations necessitating chronic corticosteroid therapy and multiple hospitalizations. To our knowledge, the persistence of symptoms years after the exposure is unique in the literature.
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PMID:Chronic reactive airway disease following acute chlorine gas exposure in an asymptomatic atopic patient. 151 50

A suicidal poisoning by intravenous administration of concentrated solution of potassium (K+) (chloride) is described in the study. A 30-year-old Caucasian female health professional was found dead in a motel. An intravenous needle was found inserted in the antecubital area in a right arm vein of the deceased. Attached to the needle, by a flexible tubing, was a 50 ml syringe four-fifths full of a clear liquid. Autopsy on the victim revealed pulmonary oedema and congestion. A routine toxicological analysis of biological samples ruled out the possibility of a drug overdose. However, the liquid from the syringe contained 1468 mmol of K+/l. Chloride ions were also present in high concentration in the liquid. The concentrations of K+ in the clear plasma and vitreous humour were 54 and 9.2 mmol/l respectively. It is suggested that the elevated level of K+ in the plasma or vitreous humour does not indicate necessarily a death due to the electrolyte. The evidence in this case is circumstantial and apparently can be expected to be so in any case where death is due to the intravenous infusion of a concentrated K+ solution.
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PMID:Poisoning associated with potassium. 380 54

1. The responses of type J pulmonary receptors (identified according to existing criteria) were studied in anaesthetized cats by recording impulses in individual vagal afferent fibres whose conduction velocity ranged from 0.8 to 7 m/sec.2. Measurements of actual latencies between insufflation of halothane or ether into the lungs and the excitation of the endings, and the latencies before and after circulatory arrest have established that the endings are located in the interstitial tissues close to the pulmonary capillaries. Mainly for this reason, the term juxta-pulmonary capillary receptors (i.e. type J receptors) has been applied to these endings in preference to the term K deflation receptors used hitherto.3. The endings were stimulated by pulmonary congestion produced by occlusion of the aorta or left a-v junction for short periods. They were markedly stimulated during pulmonary congestion following injection of alloxan (150 mg/kg) or the addition of chlorine to the inspired air. This excitation was associated with a marked rise in pulmonary artery pressure and the occurrence of pulmonary oedema. However, the actual onset of excitation occurred some time after the rise in pressure and it was in fact more closely related to fall in pulmonary compliance. The frequency of discharge averaged over about 10-20 sec (in order to take the periods of relative inactivity into account) was 7.5 impulses/sec in 10 fibres (range 0.6-19 impulses/sec; S.D. 6.3). This is intense stimulation of the endings and the congestion so produced is therefore regarded as a severe stimulus for the endings.4. The pattern of excitation was variable. In some fibres the activity consisted of periodic bursts of impulses which seemed to be set off during the deflation phase of artificial respiration, sometimes during the inflation phase. This periodic activity was not due to contraction of smooth muscle as the endings are not stimulated following injection of histamine (into the right ventricle) which is known to stimulate smooth muscles in the alveolar ducts and respiratory bronchioles.5. It is postulated that the actual stimulus for the endings is a rise in interstitial pressure or volume produced by a rise in pulmonary capillary pressure. Evidence has been gathered to show that the latter rises during muscular exercise; this rise must stimulate the endings. It was therefore postulated that stimulation of the endings should cause reflex inhibition of limb muscles (for terminating exercise).
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PMID:Mechanism of stimulation of type J pulmonary receptors. 538 24

The acute inhalation LC50 of oxalyl chloride was determined in rats following a one-hour exposure. Four groups of 10 animals per group were exposed to a concentration range of 462-2233 ppm. One set of six animals was exposed to a concentration of oxalyl chloride of 1232 ppm for one hour to evaluate the histopathological change to the lungs. The LC50 is 1840 ppm with the 95% confidence interval between 1531 ppm and 2210 ppm. Microscopically, the lungs from the treated animals exhibited acute bronchiolitis, exudate within the alveoli, and congestion. Pulmonary edema appears to contribute significantly to mortality produced by oxalyl chloride. A comparison of the acute one-hour LC50 of oxalyl chloride to that of hydrogen chloride, phosgene, phosphorus oxychloride, boron trichloride, and chlorine indicates that it shares a comparable degree of acute toxicity to hydrogen chloride and is significantly less toxic via inhalation than the latter four chemicals.
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PMID:Acute inhalation toxicology of oxalyl chloride. 787 5

In this two year retrospective review, 86 cases of chlorine gas inhalation from 49 medical facilities were treated with nebulized sodium bicarbonate on the recommendation of the Kentucky Regional Poison Center. Typical manifestations included cough, chest discomfort, shortness of breath, and wheezing. No patients developed pulmonary edema or respiratory insufficiency requiring ventilatory support. Sixty-three cases (73.3%) were exposures to chlorine producing acid/hypochlorite mixtures. Six (7.0%) were exposed to chlorine gas in industrial settings. Twelve (14.0%) were exposed to chlorine gas in swimming pool settings. Sixty-nine (80.2%) were treated and released from the emergency department. In 53 patients, clinical condition was clearly improved on emergency department discharge. Seventeen (19.8%) were admitted to the hospital. All admitted patients gradually improved and had a mean hospital stay of 1.4 days (range 1 to 3 days). No patients in this study deteriorated clinically after nebulized sodium bicarbonate use. Nebulized sodium bicarbonate appears safe and merits prospective evaluation in the therapy of chlorine gas inhalation.
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PMID:Nebulized sodium bicarbonate in the treatment of chlorine gas inhalation. 800 31

We conducted a review of the literature detailing the respiratory effects of chlorine, an extremely important but toxic halogen. Historically, the heaviest mass inhalational exposures to chlorine resulted from World War I gassing. Currently potential human exposure to chlorine inhalation occurs in a variety of settings in the workplace, as a result of inadvertent environmental releases, and even in the home due to household cleaning mishaps. Chlorine species are highly reactive; tissue injury results from exposure to chlorine, hydrochloric acid, hypochlorous acid, or chloramines. Acute, high level exposure to chlorine gas in occupational or environmental settings results in a variety of dose-related lung effects ranging from respiratory mucus membrane irritation to pulmonary edema. Pulmonary function testing can reveal either obstructive or restrictive deficits immediately following exposure, with resolution over time in the majority of cases. However, some of those exposed may demonstrate long-term persistent obstructive or restrictive pulmonary deficits or increased nonspecific airway reactivity after high level exposure to chlorine gas. Symptoms and signs following inhalation of mixtures of chlorine-containing cleaners in the home are similar to those after occupational exposures and environmental releases. Although generally less severe, these events may be extremely common. Controlled human exposure data suggest that some subjects may be more responsive to the effects of chlorine gas; epidemiologic data also indicate that certain subpopulations (e.g., smokers) may be at greater risk of adverse outcome after chlorine inhalation. Although these findings are intriguing, additional study is needed to better delineate the risk factors that predispose toward the development of long-term pulmonary sequelae following chlorine gas exposure.
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PMID:Chlorine gas exposure and the lung: a review. 836 85

We report the case of an 11-yr-old boy who developed a non-cardiogenic pulmonary edema following inhalation of chlorine gas at a swimming pool. Rapid clinical improvement was noted after i.v. administration of morphine.
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PMID:Effectiveness of morphine in non-cardiogenic pulmonary edema due to chlorine gas inhalation. 843 49


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